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At least 919 records · Page 51Linked to original sources
PubMed1982

Sequence analysis of cDNA's derived from the RNA of Sindbis virions and of defective interfering particles.

Sindbis virus generates defective interfering (DI) particles during serial high-multiplicity passage in cultured cells. These DI particles inhibit the replication of infectious virus and can be an important factor in the establishment and maintenance of persistent infection in BHK cells. In an effort to understand how these DI particles are generated and how they interfere with the replication of standard virus, we performed a partial sequence analysis of the RNA obtained from two independently isolated populations of DI particles and from two Sindbis virus variants and compared these with the RNA of the parental wild-type virus. The 3'-terminal regions of the RNAs were sequenced by the dideoxy chain terminating method. Internal regions of the RNA were examined by restriction endonuclease digestion of cDNA's made to the various RNAs and by direct chemical sequencing of 5' end-labeled restriction fragments from cDNA made to the DI RNAs. One of the variant viruses examined was originally derived from cells persistently infected with Sindbis virus for 16 months and is resistant to interference by the DI strains used. In the 3'-terminal region of the RNA from this variant, only two base changes were found; one of these occurs in the 20-nucleotide 3'-terminal sequence which is highly conserved among alphaviruses. The DI RNA sequences were found to have been produced not by a single deletional event, but by multiple deletion steps combined with sequence rearrangements; all sequences examined are derived from the plus strand of Sindbis virion RNA. Both DI RNAs had at least 50 nucleotides of wild-type sequence conserved at the 3' terminus; in addition, they both contained conserved and perhaps amplified sequences derived from the non-26S region of the genome which may be of importance in their replication and interference ability.

Base Sequence↗
PubMed1982

Interference among defective interfering particles of vesicular stomatitis virus.

Three defective interfering (DI) particles of vesicular stomatitis virus (VSV), all derived from the same parental standard San Juan strain (Indiana serotype), were used in various combinations to infect cells together with the parental virus. The replication of their RNA genomes in the presence of other competing genomes was described by the hierarchical sequence: DI 0.52 particles greater than DI 0.45 particles less than or equal to DI-T particles greater than standard VSV. The advantage of one DI particle over another was not due simply to multiplicity effects nor to the irreversible occupation of limited cellular sites. Interference, however, did correlate with a change in the ratio of plus and minus RNA templates that accumulated intracellularly and with the presence of new sequences at the 3' end of the DI genomes. DI 0.52 particles contained significantly more nucleotides at the 3' end that were complementary to those at the 5' end of its RNA than did DI-T or DI 0.45 particles. The first 45 nucleotides at the 3' ends of all of the DI RNAs were identical. VSV and its DI particles can be separated into three classes, depending on their terminal RNA sequences. These sequences suggest two mechanisms, one based on the affinity of polymerase binding and the other on the affinity of N-protein binding, that may account for interference by DI particles against standard VSV and among DI particles themselves.

Animals↗
PubMedDate not supplied

[Serous meningitis].

During the second half of the 1950s serous meningitis and other enterovirus-induced diseases played one of the leading roles in human pathology in the world. Since the introduction of oral poliomyelitis vaccine (OPV) into wide medical practice from the beginning of the 1960s and during the subsequent decades the number of epidemics and the morbidity level in enterovirus-induced diseases sharply dropped. This was probably due to the interference of enteroviruses circulating in nature and vaccine polioviruses in the intestine of vaccinated children. At the beginning of the XXI century a tendency towards a growth in the morbidity of serous meningitis of enterovirus etiology was noted. This growth was probably due to a sharp decrease in the level of revaccinations of children with OPV. At the age of 2 to 14 years, most affected by enteroviruses, children were not vaccinated with OPV and they were thus left unprotected. The materials on the epidemiology of serous meningitis and recommendations on etiological diagnosis, as well as on the patients hospitalization and the vaccination of children with OPV as a nonspecific antiepidemic measures based on the phenomenon of virus interference are presented.

Adolescent↗
PubMed2005

Avian metapneumovirus phosphoprotein targeted RNA interference silences the expression of viral proteins and inhibits virus replication.

Avian metapneumovirus (aMPV) is one of the major causes of serious respiratory infections of poultry and leads to considerable economic losses to food animal production worldwide. Here, we show that double stranded short interfering RNA (siRNA) molecules corresponding to aMPV phosphoprotein (P) gene silence P RNA and protein expression. These siRNAs broadly reduced the expression of other viral proteins in addition to P, but did not have a discernable effect on cellular protein expression. The exposure of cells to P-specific siRNAs also led to inhibition of virus replication as evidenced by marked reduction in the progeny virion titers. Taken together, the findings suggest that exogenous P silencing siRNAs can inhibit aMPV replication with potential implications in the design of novel siRNA based prophylactics.

Animals↗
PubMed1996

Inhibition of hepatitis B virus DNA polymerase by enantiomers of penciclovir triphosphate and metabolic basis for selective inhibition of HBV replication by penciclovir.

The deoxyguanosine analog penciclovir (PCV; 9-[4-hydroxy-3-hydroxymethyl-but-1-yl]guanine), has shown potent antiviral activity against herpes viruses and hepadnaviruses. Efficacy against chronic hepatitis B virus (HBV) infection has been demonstrated in an animal model and in recent clinical trials of famciclovir, the oral form of PCV. The antiviral activity of PCV is believed to be dependent on the intracellular formation of PCV-triphosphate (PCV-TP) which is presumed to inhibit HBV replication by interfering with viral DNA polymerase activity. The (S)-enantiomer is preferentially formed in herpes virus-infected cells, and is the more active against the herpes simplex virus; however, little is known about the biochemical mechanisms of PCV phosphorylation or of interference with viral replication in HBV-infected cells. Here, we report that in contrast with herpes simplex virus, the (R)-enantiomer of PCV-TP is a more potent inhibitor of HBV DNA polymerase-reverse transcriptase (pol-RT) in vitro than the (S)-enantiomer. In assays for HBV DNA pol-RT activity, in which purified viral core particles were the enzyme source, the IC50s for (R)- and (S)-enantiomers of PCV-TP were 2.5 micromol/L and 11 micromol/L, respectively. The estimated Kis for (R)- and (S)- PCV-TP were approximately 0.03 micromol/L and approximately .04 micromol/L, respectively, about 3-fold lower than the Km for deoxyguanosine triphosphate (dGTP) in the same system. In addition, we report that PCV metabolism is similar in both control (HepG2) and in HBV-transfected (2.2.15) hepatoblastoma cells in vitro, indicating that cellular enzyme(s) catalyze PCV phosphorylation. Peak PCV-TP concentrations of about .4 micromol/L were reached in both cell types in less than 12 hours, and intracellular PCV-TP was exceptionally stable with a half-life of about 18 hours. These observations provide a mechanistic basis for the potent activity of PCV against HBV.

Acyclovir↗
PubMed1986

Exclusion of superinfecting homologous virus by Sindbis virus-infected Aedes albopictus (mosquito) cells.

The infection of tissue-cultured Aedes albopictus (mosquito) cells by an alphavirus ultimately results in a persistently infected cell population which can be maintained in the laboratory for years. One characteristic of this culture is that it will not support the replication of superinfecting homologous virus. We have previously shown that mosquito cells persistently infected with Sindbis virus produce an antiviral agent which when applied to uninfected mosquito cells suppresses Sindbis virus replication. The exclusion of virus replication in the antiviral-agent-treated cells is similar to the phenomenon of homologous interference described in alphavirus-infected vertebrate cells. In this study we examined the expression of homologous interference in three lines of mosquito cells and compared the expression of homologous interference to the effects of the antiviral activity. The cell lines were found to differ in their ability to express homologous interference, and evidence suggests that the mosquito cells may suppress replication by homologous interference or by the action of the antiviral agent.

Aedes↗
PubMed1994

Three-dimensional magnetic resonance imaging of the inner ear in idiopathic sudden sensorineural hearing loss.

Five patients with idiopathic sudden sensorineural hearing loss (ISSHL) were examined by a combination of high-resolution computed tomography and special magnetic resonance imaging techniques. By three-dimensional constructive interference in steady state magnetic resonance imaging excellent visualization of the membranous labyrinth was obtained. No fibrous or osseous obliteration of the intralabyrinthine fluid spaces was observed in all investigated temporal bones. The results provide further evidence for a viral pathogenesis of ISSHL.

Audiometry, Pure-Tone↗
PubMed1993

Inhibition of herpes simplex virus type 1 DNA replication by mutant forms of the origin-binding protein.

The herpes simplex virus type 1 (HSV-1) origin-binding protein (OBP) is a sequence-specific DNA binding protein encoded by gene UL9 which interacts with the viral origins of DNA replication and also exhibits DNA helicase activity. Sequence-specific DNA binding activity has previously been shown to reside within the C-terminal 317 amino acids, and when expressed alone, this domain exerts a dominant inhibitory effect on HSV-1 DNA synthesis. We have tested several UL9 gene mutants for ability to support or interfere with viral DNA replication. Mutants affected in an ATP binding motif presumed to be associated with DNA helicase activity (ATP-), or defective in origin binding (OBP-) were unable to support replication in a transient assay for HSV-1 origin-dependent DNA synthesis. When the products were screened for their ability to interfere with replication, the ATP- but not the OBP- mutant was inhibitory. Introduction of a mutation which abolished origin-binding activity into the isolated C-terminal fragment also removed the ability to interfere. The C-terminal fragment retained inhibitory activity when the wild-type (wt) protein was specified by a plasmid in which an OBP recognition site within the UL9 gene coding region had been mutated so as to prevent binding without affecting the encoded amino acids. These results suggest that in this assay inhibition of DNA synthesis probably results primarily from competition between mutant and wt forms of OBP for binding to the viral replication origins. The infectivity of HSV-1 DNA in co-transfection experiments was greatly reduced by mutant UL9 proteins which interfered with origin-dependent DNA replication and also by high level expression of the wt polypeptide.

Animals↗
PubMed2004

RNAi, a new therapeutic strategy against viral infection.

RNA interference (RNAi) is an adaptive defense mechanism triggered by double-stranded RNA (dsRNA). It is a powerful reverse genetic tool that has been widely employed to silence gene expression in mammalian and human cells. RNAi-based gene therapies, especially in viral diseases have become more and more interesting and promising. Recently, small interfering RNA (siRNA) can be used to protect host from viral infection, inhibit the expression of viral antigen and accessory genes, control the transcription and replication of viral genome, hinder the assembly of viral particles, and display influences in virus-host interactions. In this review, we attempt to present recent progresses of this breakthrough technology in the above fields and summarize the possibilities of siRNA-based drugs.

Animals↗